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<b>Background/Objective</b> <p>Although chronic subdural hematoma/fluid collection (CSDH/FC) is a common disease, its pathogenesis is not yet completely understood. Traditionally, it has been thought to result from blood pooling in a subdural space following bridging vein rupture and inflammatory changes. However, recent anatomical findings challenge this view, suggesting that the area previously considered “subdural space" is instead filled with a dural border cell layer (DBCL), a specialized cell layer involved in cerebrospinal fluid absorption and drainage. In this study, we reinterpreted CSDH/FC as a DBCL effusion rather than a true subdural pathology and highlights the importance of DBCL vascular dynamics, thereby reshaping the understanding of its pathophysiology, diagnosis, and management. For consistency and clarity, however, the conventional term “subdural” is retained throughout this manuscript despite its anatomical inaccuracy.</p> <b>Methods</b> <p>We retrospectively reviewed imaging and clinical data for 24 CSDH/FC cases lacking obvious high-attenuation components on initial CT scans, treated between April 2022 and January 2024. Contrast enhancement in CSDH/FC was assessed in four cases with dual-energy CT (DECT) and in two cases with MRI. </p> <b>Results</b> <p>Observed background factors included brain atrophy in 5 cases, history of head trauma in 18, prior shunt surgery for idiopathic normal pressure hydrocephalus in one, previous CSDH/FC evacuation in 4, and spontaneous intracranial hypotension in 2. Exudation of contrast media into CSDH/FC was confirmed in all contrast-enhanced cases. </p> <b>Conclusions</b> <p>CSDH/FC is an accumulation of blood components within the DBCL, which is the deepest layer of the dura mater. &#xa0;Factors like brain atrophy and reduced CSF volume may increase DBCL capillary permeability, enabling blood components to collect within the DBCL and potentially progress to CSDH/FC. Contrast exudation observed by DECT and MRI supports this hypothesis, offering insights into the development of CSDH/FC.</p>

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Pathogenesis of Chronic Subdural Hematoma/Fluid Collection in Adults from the Perspective of the Dural Border Cell Layer

  • 期刊论文

  • 发表日期：

    2025年7月21日

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  • Akinobu Osame,
  • Hidetsuna Utsunomiya,
  • Yukie Higuma,
  • Hiroshi Toyoshima,
  • Rikiya Nakashima,
  • Yuki Kozaki,
  • Kenji Fukuda,
  • Shuji Hayashi,
  • Toru Inoue

摘要

Background/Objective

Although chronic subdural hematoma/fluid collection (CSDH/FC) is a common disease, its pathogenesis is not yet completely understood. Traditionally, it has been thought to result from blood pooling in a subdural space following bridging vein rupture and inflammatory changes. However, recent anatomical findings challenge this view, suggesting that the area previously considered “subdural space" is instead filled with a dural border cell layer (DBCL), a specialized cell layer involved in cerebrospinal fluid absorption and drainage. In this study, we reinterpreted CSDH/FC as a DBCL effusion rather than a true subdural pathology and highlights the importance of DBCL vascular dynamics, thereby reshaping the understanding of its pathophysiology, diagnosis, and management. For consistency and clarity, however, the conventional term “subdural” is retained throughout this manuscript despite its anatomical inaccuracy.

Methods

We retrospectively reviewed imaging and clinical data for 24 CSDH/FC cases lacking obvious high-attenuation components on initial CT scans, treated between April 2022 and January 2024. Contrast enhancement in CSDH/FC was assessed in four cases with dual-energy CT (DECT) and in two cases with MRI.

Results

Observed background factors included brain atrophy in 5 cases, history of head trauma in 18, prior shunt surgery for idiopathic normal pressure hydrocephalus in one, previous CSDH/FC evacuation in 4, and spontaneous intracranial hypotension in 2. Exudation of contrast media into CSDH/FC was confirmed in all contrast-enhanced cases.

Conclusions

CSDH/FC is an accumulation of blood components within the DBCL, which is the deepest layer of the dura mater.  Factors like brain atrophy and reduced CSF volume may increase DBCL capillary permeability, enabling blood components to collect within the DBCL and potentially progress to CSDH/FC. Contrast exudation observed by DECT and MRI supports this hypothesis, offering insights into the development of CSDH/FC.